Hemodialysis was advanced as a life sustaining therapy for end-stage renal failure, when in about 1925 it was discovered that a thin film of re-constituted cellulose (cellophane®) had the ability to separate chemical substances while in solution by means of their unequal diffusion through a permeable membrane. This phenomenon performed particularly well with blood to differentially separate out urea molecules. Over the years there have been many changes to incrementally improve the hemodialysis process. The fundamentals, however, remained the same. Hemodialysis essentially mimics the kidney function of processing whole blood, however, man-made membranes are a poor substitute for one's kidney function.
Whole blood is made up of four major components: a) red blood cells, b) white blood cells, c) platelets, and d) plasma fluid. Since the toxins or ureas to be removed are in the plasma solution liquid portion of the whole blood, the cells just go along for the ride. The cells are also very fragile, so although they do not participate in the dialysis process directly, they do come in contact with the dialyzing membrane. Their presence, therefore, dominates the rate at which hemodialysis can proceed. Generally, a hemodialysis process takes place over a four to six hour time period for treatment and generally such treatments would be required 3 times per week. The dialyzer is also patient specific.
During each treatment the patient's total blood volume is drawn from the patient, passed through a urea separation device and returned in a continuous fashion to the patient.
Many clinical complications arise because of the need to remove urea and other toxins while the fragile cells are present: of these, compatibility of the dialyzer membranes and whole blood is of major concern. Both proteins and cells adhere to the membrane surface. This contact, in turn, causes a number of deleterious responses, which resemble those of assaults to the patient's immune system in the form of a severe allergic reactions, serious complement activation in the C3 C5 region, to which the body reacts as if invaded by a foreign pathogen. The responses are numerous and in some instances life threatening. They include                Platelet adhesion, agglomeration and damage        Thrombosis and erythrocyte adhesion        Complement activation (C3/C5)        White cell activation (granulocytes, leukocytes, monocytes)        
The clinical manifestations are also numerous and in some cases lead to morbidity and mortalities.                Anemia        Hypoxemia        Organ damage        Blood poisoning (Septicemia)        Infections, lumen and surface penetration        Malignancies        Leukopenia        